|Name 5 characteristics of the metabolic syndrome||
atherogenic lipid patterns
insulin resistance or diabetes
pro-inflammatory state, ie C-reactive protein
|Describe stable angina||
Chest pain precipitated by exertion, relieved by rest or vasodilators.
|Describe unstable angina||
Chest pain that is prolonged or recurrent at rest.
|Describe Prinzmetal angina||
Intermittent chest pain at rest, usually caused by vasospasm.
|The two patterns of myocardial ischemic necrosis? Describe them.||
Transmural: entire ventricular wall from endo- to epicardium.
Subendocardial: limited to interior one third of ventricular wall
|Name 6 complications of myocardial infarction.||
Arrhythmia: common cause of death in first hours after MI
Heart failure: depends on MI size
Myocardial rupture: risk highest 4-7 days after MI
Papillary muscle rupture
Mural thrombosis: forms over infarct in heart, can embolize
|Timeline of GROSS morphological changes in acute myocardial infarction?||
< 12 hrs: no gross changes
24 hrs: swelling, pale or red brown infarct with surrounding hyperemia
7 days: yellow infarcted area with red border
10 days: red vascular connective tissue gradually replaces necrotic tissue
5 weeks: pallor of infarct due to fibrosis
3-6 months: gray-white scar
|Timeline of MICROSCOPIC morphological changes in acute myocardial infarction?||
< 6hrs: none
12-24hrs: nuclei disappear, striations lost, neutrophils infiltrate, coagulative necrosis apparent
3 days: macrophages replace neutrophils, phagocytose debris
7 days: growth of fibroblasts and new vessels in the lesion
2-4 weeks: collagen and matrix synthesis
>5 weeks: progressive fibrosis replaces lesion
|When do LDH, troponin, and CK-MB each peak in acute myocardial infarction?||
LDH peaks at 3 days and persists.
Troponin peaks at 24 hours and persists.
CK-MB peaks at 24 hours and tapers to zero.
|Rheumatic fever: etiology||
Immunologic disease. Streptococcal antigens elicit an antibody response that is reactive to human heart and other tissues.
|Rheumatic fever: name and characteristics of the classic histologic lesion?||
Focal interstitial myocardial inflammation with collagen, fibrinoid material, multinucleated giant cells, and large myocytes.
|Rheumatic fever: how long after what infection? What lab sign indicates recent infection?||
1-4 weeks after Group A beta hemolytic streptococcus infection. Elevated anti-streptolysin (ASO) indicates recent infection.
|Rheumatic fever: non-cardiac manifestations||
Fever, malaise, elevated ESR, arthralgias/arthritis/migratory polyarthritis, subcutaneous nodules, erythema marginatum, Sydenham chorea.
|Rheumatic fever: cardiac manifestations||
Pancarditis (all 3 layers).
Non-friable mitral and aortic vegetations, which after healing cause fibrosis, calcification, and deformation of the values. Chordae tendineae are also thickened and shortened.
|Organisms causing acute vs subacute bacterial endocarditis||
Acute: staph aureus (also beta hemolytic strep and pneumococcus)
Subacute: strep viridans (also enterococcus, HACEK organisms)
|Complications of infective endocarditis?||
Distal embolization to brain or other tissues can lead to septic infarcts.
Renal glomeruli involvement due to immune complex disease or septic emboli.
|Suspect what if tricuspid valve is involved in infective endocarditis?||
IV drug use. 50% of cases of endocarditis in this population have tricuspid involvement.
|Risk factors for infectious endocarditis?||
Congenital heart disease
Preexisting valvular heart disease
IV drug use
|What is nonbacterial thrombotic endocarditis associated with? What are its complications?||
Metastatic cancer and other wasting disorders.
Valve deposits are sterile and made of fibrin... as a result emboli are sterile, not septic.
|What is Libman-Sacks endocarditis?||
Occurs in SLE, is characterized by small fibrin vegetations forming on either or both sides of the valve leaflets.
|What is endocarditis of the carcinoid syndrome?||
Caused by secretory products of carcinoid tumors such as serotonin and other vasoactive peptides and amines. They cause endocarditis resulting in thickened endocardial plaques, usually in the RIGHT of the heart because these substances are inactivated in the pulmonary circulation.
|Most common valvular lesion?||
Mitral prolapse (7% of population)
|Characteristic sound of mitral prolapse?||
Systolic murmur with midsystolic click.
|Causes of mitral stenosis?||
Almost always rheumatic heart disease.
|Causes of aortic stenosis?||
Age related calcific stenosis
Congenital bicuspid valve
|Causes of aortic regurgitation?||
Nondissecting aortic aneurysm
Rheumatic heart disease
Syphilitic aortitis with dilation of valve ring
|Coarctation of aorta is more common in what syndrome?||
Turner's syndrome (monosomy X)
|Congenital rubella syndrome includes what fetal defects?||
Cardiovascular (PDA and others)
|What drug keeps PDA open? what drug closes it?||
Prostaglandin keeps it open.
Indomethacin closes it.
|Name three conditions associated with dilated cardiomyopathy.||
Alcoholism, thiamine deficiency, prior myocarditis.
|What is a common cause of restrictive cardiomyopathy?||
|what are the morphological changes seen in hypertrophic cardiomyopathy?||
hypertrophy of all chamber walls especially the ventricular septum.
Disoriented tangled and hypertrophied myocardial fibers.
Left ventricular outflow obstruction.
|What is the inheritance of hypertrophic cardiomyopathy?||
Usually autosomal dominant
|what is the most common cause of myocarditis?||
|what is the most common tumor of the heart?||
|What is cor pulmonale? Name one common cause.||
Cor pulmonale is right ventricular hypertrophy or dilation secondary to lung disease or primary disease of pulmonary vasculature such as primary pulmonary hypertension.
Emphysema is a common cause.